Vascular prostaglandin I2 (PGI2) is a potent inhibitor of platelet aggregation and keeps the vascular wall non-thrombotic. Since aspirin inhibits the synthesis of both thromboxane A2 and PGI2, the usefulness of this drug in thrombosis prevension is subject for discussion.
In this report, we studied first the assay method of PGI2 using platelet aggregation test, and then the effect of aspirin on platelet MDA and vascular PGI2 formation.
One hundred mg of aortic rings (approximately 3mg/ring) were indcubated in 100μl of 50mMol. tris-buffer (pH7.5) for 5 minutes at room temperature. The supernate contained platelet aggregation inhibiting activity equivalent to 200ng/ml of PGI2. The activity was stable for 3 hours at 0°C. PGI2 released from each of three equal sized portions of aorta cut into rings each weighing around 2.3, 3.3 or 7.7mg, respectively, were same.
Vascular PGI2 formation was almost completely inhibited for at least 12 hours after the administration of aspirin (0.3g), and returned to initial level after 24 hours. But platelet MDA formation was markedly inhibited even 48 hours after the administration of aspirin. This means that the inhibitory effect of a single dose of aspirin lasts longer on platelet than on vascular PG synthesis.
From these data, it is suggested that a dose of aspirin which inhibits platelet cyclooxygenase completely with slight inhibition of vascular cyclooxygenase may exist.
